肺塞栓症例での，t-PA投与後の凝固線溶血管分子マーカーの変動

The Changes of Molecular Markers for Hemostatic Activation after t-PA Therapy in Case of Pulmonary Embolism

　肺塞栓症にtissue plasminogen activator（t-PA）を投与し，凝固線溶血管分子マーカーの変動を経時的に観察した．症例は70歳，男性．肺動脈造影にて，右上幹と左舌区枝の欠損を認めた．t-PA 2000万単位の肺動脈内注入で，血流の著明な改善をみた．t-PAの投与直前，投与中，投与終了時と終了30分後および1,2,6,24時間後と第5,7病日に肘静脈より採血し，thrombin-antithrombin Ⅲ complex（TAT），plasmin-α₂ plasmin inhibitor complex（PIC），throm-bomodulin（TM）を測定した．TATはt-PA投与30分後より6時間まで，正常値の30倍程度に上昇し，既報告の心筋梗塞例より高値の持続が明らかに長かった．PICは投与中，前値の3倍程度に上昇し，以後心筋梗塞例と同程度に漸減して6時間で前値近くに低下した．TMは経過を通じて常に高値であり，血栓溶解療法にかかわらず，肺梗塞の急性期においては比較的長期間高値が持続していたことが注目される．

We observed the changes of molecular markers for hemostatic activation in a patient with acute pulmo-nary embolism treated with 2×10⁷ unit tissue plas-minogen activator (t-PA). Blood samples were obtained before, just after, at 30 min, 1, 2, 6, and 24 hours after the infusion. Molecular markers included thrombin- antithrombin Ⅲ complex (TAT), plas-minogen-alpha 2 plasmin inhibitor complex (PIC), and thrombomodulin (TM). Marked elevation of TAT was observed from immediately after the t-PA infusion to 6 hours after, although it had been observed for only 1 hour in our previous report on the cases of acute myocardial infarction.